Journal
IMMUNITY
Volume 12, Issue 5, Pages 557-568Publisher
CELL PRESS
DOI: 10.1016/S1074-7613(00)80207-1
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Funding
- NHLBI NIH HHS [R01 HL-45635] Funding Source: Medline
- NIDDK NIH HHS [R01 DK48605] Funding Source: Medline
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Mast cells generated from Rac2-deficient (-/-) mice demonstrated defective actin-based functions, including adhesion, migration, and degranulation. Rac2(-/-) mast cells generated lower numbers and less mast cell colonies in response to growth factors and were deficient in vivo. Rac2(-/-) mast cells demonstrated a significant reduction in growth factor-induced survival, which correlated with the lack of activation of Akt and significant changes in the expression of the Bcl-2 family members BAD and Bcl-X-L, in spite of a 3-fold induction of Rac1 protein. These results suggest that Rac2 plays a unique role in multiple cellular functions and describe an essential role for Rac2 in growth factor-dependent survival and expression of BAD/Bcl-X-L.
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